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Short sleep duration and decreased sleep quality are emerging risk factors for obesity and its associated morbidities. Chronotype, an attribute that reflects individual preferences in the timing of sleep and other behaviors, is a continuum from morningness to eveningness. The importance of chronotype in relation to obesity is mostly unknown. Evening types tend to have unhealthy eating habits and suffer from psychological problems more frequently than Morning types, thus we hypothesized that eveningness may affect health parameters in a cohort of obese individuals reporting sleeping less than 6.5 hours per night. BASELINE DATA FROM OBESE (BMI: 38.5±6.4 kg/m(2)) and short sleeping (5.8±0.8 h/night by actigraphy) participants (n = 119) of the Sleep Extension Study were analyzed (www.ClinicalTrials.gov, identifier NCT00261898). Assessments included the Horne and Ostberg Morningness-Eveningness questionnaire, a three-day dietary intake diary, a 14-day sleep diary, 14 days of actigraphy, and measurements of sleep apnea. Twenty-four hour urinary free cortisol, 24 h urinary norepinephrine and epinephrine levels, morning plasma ACTH and serum cortisol, fasting glucose and insulin, and lipid parameters were determined. Eveningness was associated with eating later in the day on both working and non-working days. Progression towards eveningness was associated with an increase in BMI, resting heart rate, food portion size, and a decrease in the number of eating occasions and HDL-cholesterol. Evening types had overtly higher 24 h urinary epinephrine and morning plasma ACTH levels, and higher morning resting heart rate than Morning types. In addition, Evening types more often had sleep apnea, independent of BMI or neck circumference. Eveningness was associated with eating later and a tendency towards fewer and larger meals and lower HDL-cholesterol levels. In addition, Evening types had more sleep apnea and higher stress hormones. Thus, eveningness in obese, chronically sleep-deprived individuals compounds the cardiovascular risk associated with obesity.

Background: Long term non-invasive ventilation (NIV) reduces morbidity and mortality in patients with neuromuscular and chest wall disease with hypercapnic ventilatory failure, but preventive use has not produced benefit in normocapnic patients with Duchenne muscular dystrophy. Individuals with nocturnal hypercapnia but daytime normocapnia were randomised to a control group or nocturnal NIV to examine whether nocturnal hypoventilation is a valid indication for NIV. Methods: Forty eight patients with congenital neuromuscular or chest wall disease aged 7–51 years and vital capacity <50% predicted underwent overnight respiratory monitoring. Twenty six with daytime normocapnia and nocturnal hypercapnia were randomised to either nocturnal NIV or to a control group without ventilatory support. NIV was started in the control group if patients fulfilled preset safety criteria. Results: Peak nocturnal transcutaneous carbon dioxide tension (Tcco2) did not differ between the groups, but the mean (SD) percentage of the night during which Tcco2 was >6.5 kPa decreased in the NIV group (−57.7 (26.1)%) but not in controls (−11.75 (46.1)%; p = 0.049, 95% CI −91.5 to −0.35). Mean (SD) arterial oxygen saturation increased in the NIV group (+2.97 (2.57)%) but not in controls (−1.12 (2.02)%; p = 0.024, 95% CI 0.69 to 7.5). Nine of the 10 controls failed non-intervention by fulfilling criteria to initiate NIV after a mean (SD) of 8.3 (7.3) months. Conclusion: Patients with neuromuscular disease with nocturnal hypoventilation are likely to deteriorate with the development of daytime hypercapnia and/or progressive symptoms within 2 years and may benefit from the introduction of nocturnal NIV before daytime hypercapnia ensues.

To examine dose-dependent effects of mandibular advancement on collapsibility of the passive pharynx and sleep-disordered breathing (SDB). Prospective, randomized study. University hospital. Thirty-seven adult patients with SDB. Oral appliances with 2-, 4-, and 6-mm advancement of the mandible. Overnight oximetry was performed with and without oral appliances. Each 2-mm mandibular advancement coincided with approximately 20% improvement in number and severity of nocturnal desaturations. Percentages of patients producing a > 50% improvement rate of the number of desaturations were 25%, 48%, and 65% with use of oral appliances with 2-, 4-, and 6-mm mandibular advancement, respectively. Static pharyngeal mechanics were evaluated in six completely paralyzed patients with SDB under general anesthesia with and without the oral appliances. Advancement of mandibular position was found to produce dose-dependent closing pressure reduction of all pharyngeal segments. Normalization of nocturnal oxygenation was associated with negative closing pressure, especially at the velopharynx. We conclude that improvement of both nocturnal oxygenation and pharyngeal collapsibility significantly depends on the mandibular position.

Backgrounds To explain the excess cardiovascular mortality observed in the SERVE-HF study, it was hypothesized that the high-pressure ASV default settings used lead to inappropriate ventilation, cascading negative consequences (i.e. not only pro-arrythmogenic effects through metabolic/electrolyte abnormalities, but also lower cardiac output). The aims of this study are: i) to describe ASV-settings for long-term ASV-populations in real-life conditions; ii) to describe the associated minute-ventilations (MV) and therapeutic pressures for servo-controlled-flow versus servo-controlled-volume devices (ASV-F Philips®-devices versus ASV-V ResMed®-devices). Methods The OTRLASV-study is a cross-sectional, 5-centre study including patients who underwent ASV-treatment for at least 1 year. The eight participating clinicians were free to adjust ASV settings, which were compared among i) initial diagnosed sleep-disordered-breathing (SBD) groups (Obstructive-Sleep-Apnea (OSA), Central-Sleep-Apnea (CSA), Treatment-Emergent-Central-Sleep-Apnea (TECSA)), and ii) unsupervised groups ( k -means clusters). To generate these clusters, baseline and follow-up variables were used (age, sex, body mass index (BMI), initial diagnosed Obstructive-Apnea-Index, initial diagnosed Central-Apnea-Index, Continuous-Positive-Airway-Pressure used before ASV treatment, presence of cardiopathy, and presence of a reduced left-ventricular-ejection-fraction (LVEF)). ASV-data were collected using the manufacturer’s software for 6 months. Results One hundred seventy-seven patients (87.57% male) were analysed with a median (IQ 25–75 ) initial Apnea-Hypopnea-Index of 50 (38–62)/h, an ASV-treatment duration of 2.88 (1.76–4.96) years, 61.58% treated with an ASV-V. SDB groups did not differ in ASV settings, MV or therapeutic pressures. In contrast, the five generated k -means clusters did (generally described as follows: (C1) male-TECSA-cardiopathy, (C2) male-mostly-CSA-cardiopathy, (C3) male-mostly-TECSA-no cardiopathy, (C4) female-mostly-elevated BMI-TECSA-cardiopathy, (C5) male-mostly-OSA-low-LVEF). Of note, the male-mostly-OSA-low-LVEF-cluster-5 had significantly lower fixed end-expiratory-airway-pressure (EPAP) settings versus C1 ( p  = 0.029) and C4 ( p  = 0.007). Auto-EPAP usage was higher in the male-mostly-TECSA-no cardiopathy-cluster-3 versus C1 ( p  = 0.006) and C2 ( p  < 0.001). MV differences between ASV-F ( p  = 0.002) and ASV-V ( p  < 0.001) were not homogenously distributed across clusters, suggesting specific cluster and ASV-algorithm interactions. Individual ASV-data suggest that the hyperventilation risk is not related to the cluster nor the ASV-monitoring type. Conclusions Real-life ASV settings are associated with combinations of baseline and follow-up variables wherein cardiological variables remain clinically meaningful. At the patient level, a hyperventilation risk exists regardless of cluster or ASV-monitoring type, spotlighting a future role of MV-telemonitoring in the interest of patient-safety. Trial registration The OTRLASV study was registered on ClinicalTrials.gov (Identifier: NCT02429986 ). 1 April 2015.

Sleep apnea is a potential risk factor for Alzheimer's Disease (AD). Associations between sleep apnea and elevated AD biomarkers like amyloid beta (Aβ) and p-tau have been reported, but it is unclear if or how sleep apnea influences the connection between the two. The link between sleep apnea and AD also has not been extensively studied in the context of relevant demographic, sociocultural, and common genetic factors. Therefore, we assessed the moderating effects of sleep apnea on the association between Aβ-PET and plasma p-tau217 and whether this moderation differed based on sex, ethnicity, or APOE e4 carrier status. We studied 1Florida ADRC participants (N = 288) with normal cognition, mild cognitive impairment, or dementia (Table 1). Presence or absence of sleep apnea was determined from the National Alzheimer's Coordinating Center Health History. All participants had plasma samples analyzed for p-tau217 (ALZPath) and completed Aβ-PET with [18F] florbetaben or florbetapir. Global standardized uptake value ratio (SUVR; whole cerebellum reference) was calculated and converted to the Centiloid (CL) scale. We used multiple linear regression to assess the interaction of Aβ-PET and sleep apnea status on plasma p-tau217, controlling for age, sex, and CDR sum of boxes. To determine whether sleep apnea moderator effects differed by APOE e4 carrier status, sex, or ethnicity (Hispanic/Latino vs. non-Hispanic/Latino), we employed three-way interactions. Sleep apnea moderated Aβ-PET associations with p-tau217 (β = 0.26, p = .022; Figure 1), such that greater amyloid burden related more strongly to higher plasma p-tau217 in those with sleep apnea versus without. A significant three-way interaction of Aβ-PET x sleep apnea x ethnicity on plasma p-tau217 (β = -0.52, p = .024; Figure 2) revealed that sleep apnea only moderated this association in non-Hispanic/Latino participants. Sleep apnea moderation was not dependent on sex or APOE e4 carrier status. Addressing sleep apnea as a modifiable risk factor may promote slowing or resistance to AD. Larger and longitudinal studies are needed to comprehensively examine sleep apnea in older adults. Exploring sleep apnea effects in more representative samples with consideration of social and structural determinants of brain health will help clarify the role of sleep on AD onset and progression.

It is well established that sleep-disordered breathing (SDB) is independently associated with insulin resistance, glucose intolerance, and type 2 diabetes mellitus. However, data on whether SDB alters in vivo kinetics of glucose and insulin are lacking. The primary goal of this study was to use the frequently sampled intravenous glucose tolerance test (FSIVGTT) in subjects with and without SDB to model the in vivo kinetics of glucose and insulin. Minimal model analysis of the FSIVGTT data was used to derive parameters of insulin sensitivity, glucose effectiveness (a measure of the ability of glucose to mediate its own disposal), and pancreatic beta-cell function. A total of 118 nondiabetic subjects underwent polysomnography, the FSIVGTT, and body composition measurements including determination of percent body fat. Compared with normal subjects (apnea-hypopnea index < 5 events/h), those with mild, moderate, and severe SDB displayed a 26.7, 36.5 and 43.7% reduction in insulin sensitivity, respectively, independent of age, sex, race, and percent body fat. The disposition index, an integrated measure of pancreatic beta-cell function, was also reduced in patients with moderate to severe SDB. The decrease in insulin sensitivity and the disposition index were correlated with the average degree of oxyhemoglobin desaturation. In contrast, glucose effectiveness was negatively correlated with the frequency of respiratory event-related arousals. The results of this study suggest that, independent of adiposity, SDB is associated with impairments in insulin sensitivity, glucose effectiveness, and pancreatic beta-cell function. Collectively, these defects may increase the risk of glucose intolerance and type 2 diabetes mellitus in SDB.

The prevalence of metabolic syndrome (MS) has increased rapidly in Taiwan and worldwide. We aim to determine the association between sleep-disordered breathing (SDB) and MS in a Chinese general population. This case-control study recruited subjects who have undergone a prospective electrocardiogram-based cardiopulmonary coupling (CPC) sleep spectrogram as part of the periodic health check-ups at the National Taiwan University Hospital. Comprehensive anthropometrics, blood biochemistry, prevalence of MS and its individual components were compared with Bonferroni correction between 40 subjects with SDB, defined as the CPC-derived apnea-hypopnea index (CPC-AHI) >5 event/hour and 80 age- and sex-matched controls, defined as CPC-AHI <1 event/hour. MS was diagnosed based on the Adult Treatment Panel III, with a modification of waist circumference for Asians. Subjects with SDB were more obese with larger waist circumferences (95.1±12.9 vs. 87.3±6.9, P < .001) and borderline higher BMI (27.0±4.9 vs. 24.3±2.5, P = .002). Waist circumference was independently associated with the presence of SDB after adjustment for BMI, systolic blood pressure and fasting blood glucose in multiple regression analyses. Subjects with SDB had a higher prevalence of central obesity (72.5% vs. 42.5%, P = .002), hyperglycemia (45.0% vs. 26.3%, P = .04), MS (45.0% vs. 22.5%, P = .01) and number of MS components (2.4 ± 1.6 vs. 1.7 ± 1.4, P = .01) than the control group. Waist circumference was significantly correlated with both CPC-AHI (r = .492, P = .0013) and PSG-AHI (r = .699, P < .0001) in the SDB group. SDB was associated with a higher prevalence of MS and its individual components, notably central obesity, in a Chinese general population. Large-scale screening of high risk population with MS to identify subjects with SDB for appropriate management is warranted.

Obstructive sleep apnea (OSA), characterized by intermittent hypoxia/reoxygenation (IHR), is associated with atherosclerosis. Polymorphonuclear leukocytes (PMNs) are implicated in atherogenesis by producing oxidizing radicals and proteolytic enzymes during PMN-endothelium interactions. PMN apoptosis is a fundamental, injury-limiting mechanism, which prevents their destructive potential. To determine whether PMN apoptosis and expression of adhesion molecules are affected by OSA and IHR in vitro. Apoptosis and expression of adhesion molecules were assessed in whole blood PMNs by flow cytometry, verified by various culture conditions, and morphology. These were complemented by exposing whole blood and purified PMNs to IHR and to sustained hypoxia in vitro. This study demonstrates for the first time that, in patients with moderate to severe OSA, PMN apoptosis is delayed. Apoptosis was attenuated in patients with an apnea-hypopnea index (AHI) of more than 15, determined by decreased expression of low-CD16/annexin-V-positive PMNs, by lowered caspase-3 activity and nuclear condensation. Concomitantly, selectin-CD15 expression was increased in a severity-dependent manner in patients with moderate to severe OSA having an AHI greater than 15. The percentage of apoptotic PMNs was negatively correlated with OSA severity, determined by AHI, and positively with CD15 expression. In nasal continuous positive airway pressure-treated patients, CD15 expression was attenuated and low CD16 was increased, whereas omitting nasal continuous positive airway pressure for a single night increased CD15 expression and decreased the percentage of low CD16. IHR in vitro delayed PMN apoptosis as well. Decreased apoptosis and increased expression of adhesion molecules were noted in OSA PMNs. Although adhesion molecules may facilitate increased PMN-endothelium interactions, decreased apoptosis may further augment these interactions and facilitate free radical and proteolytic enzyme release.

Pulmonary arterial hypertension (PAH) is frequently complicated by sleep disordered breathing (SDB), and previous studies have largely focused on hypoxemic SDB. Even though nocturnal hypercapnia was shown to exacerbate pulmonary hypertension, the clinical significance of nocturnal hypercapnia among PAH patients has been scarcely investigated. Seventeen patients with PAH were identified from 246 consecutive patients referred to Kyoto University Hospital for the evaluation of lung transplant registration from January 2010 to December 2017. Included in this study were 13 patients whose nocturnal transcutaneous carbon dioxide partial pressure (PtcCO2) monitoring data were available. Nocturnal hypercapnia was diagnosed according to the guidelines of the American Academy of Sleep Medicine. Associations of nocturnal PtcCO2 measurements with clinical features, the findings of right heart catheterization and pulmonary function parameters were evaluated. Nocturnal hypercapnia was diagnosed in six patients (46.2%), while no patient had daytime hypercapnia. Of note, nocturnal hypercapnia was found for 5 out of 6 patients with idiopathic PAH (83.3%). Mean nocturnal PtcCO2 levels correlated negatively with the percentage of predicted total lung capacity (TLC), and positively with cardiac output and cardiac index. Nocturnal hypercapnia was prevalent among advanced PAH patients who were waiting for lung transplantation, and associated with %TLC. Nocturnal hypercapnia was associated with the increase in cardiac output, which might potentially worsen pulmonary hypertension especially during sleep. Further studies are needed to investigate hemodynamics during sleep and to clarify whether nocturnal hypercapnia can be a therapeutic target for PAH patients.

Type 2 diabetes (T2D) is an independent risk factor for sleep breathing disorders. However, it is unknown whether T2D affects daily somnolence and quality of sleep independently of the impairment of polysomnographic parameters. A case-control study including 413 patients with T2D and 413 non-diabetic subjects, matched by age, gender, BMI, and waist and neck circumferences. A polysomnography was performed and daytime sleepiness was evaluated using the Epworth Sleepiness Scale (ESS). In addition, 135 subjects with T2D and 45 controls matched by the same previous parameters were also evaluated through the Pittsburgh Sleep Quality Index (PSQI) to calculate sleep quality. Daytime sleepiness was higher in T2D than in control subjects (p = 0.003), with 23.9% of subjects presenting an excessive daytime sleepiness (ESS>10). Patients with fasting plasma glucose (FPG ≥13.1 mmol/l) were identified as the group with a higher risk associated with an ESS>10 (OR 3.9, 95% CI 1.8-7.9, p = 0.0003). A stepwise regression analyses showed that the presence of T2D, baseline glucose levels and gender but not polysomnographic parameters (i.e apnea-hyoapnea index or sleeping time spent with oxigen saturation lower than 90%) independently predicted the ESS score. In addition, subjects with T2D showed higher sleep disturbances [PSQI: 7.0 (1.0-18.0) vs. 4 (0.0-12.0), p<0.001]. The presence of T2D and high levels of FPG are independent risk factors for daytime sleepiness and adversely affect sleep quality. Prospective studies addressed to demonstrate whether glycemia optimization could improve the sleep quality in T2D patients seem warranted.